Background

Spontaneous bacterial peritonitis (SBP) is an acute bacterial infection of ascitic fluid. Generally, no source of the infecting agent is easily identifiable, but contamination of dialysate can cause the condition among those receiving peritoneal dialysis (PD).

Spontaneous bacterial peritonitis occurs in both children and adults and is a well-known and ominous complication in patients with cirrhosis.
[1] Of patients with cirrhosis who have spontaneous bacterial peritonitis, 70% are Child-Pugh class C. In these patients, the development of spontaneous bacterial peritonitis is associated with a poor long-term prognosis. Patients with cirrhosis who develop spontaneous bacterial peritonitis in the face of septic shock are at high risk of mortality.

Once thought to occur only in those individuals with alcoholic cirrhosis, spontaneous bacterial peritonitis is now known to affect patients with cirrhosis from any cause. In addition, spontaneous bacterial peritonitis can occur as a complication of any disease state that produces the clinical syndrome of ascites, such as heart failure and Budd-Chiari syndrome. Children with nephrosis or systemic lupus erythematosus who have ascites have a high risk of developing spontaneous bacterial peritonitis.

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Pathophysiology

The mechanism for bacterial inoculation of ascites has been the subject of much debate since Harold Conn first recognized the disorder in the 1960s. Enteric organisms have traditionally been isolated from more than 90% of infected ascites fluid in spontaneous bacterial peritonitis, suggesting that the GI tract is the source of bacterial contamination.

The preponderance of enteric organisms, in combination with the presence of endotoxin in ascitic fluid and blood, once favored the argument that spontaneous bacterial peritonitis was due to direct transmural migration of bacteria from an intestinal or hollow organ lumen, a phenomenon called bacterial translocation. However, experimental evidence suggests that direct transmural migration of microorganisms might not be the cause.

An alternative proposed mechanism for bacterial inoculation of ascites is hematogenous transmission in combination with an impaired immune system. Nonetheless, the exact mechanism of bacterial displacement from the GI tract into ascites fluid remains controversial.

A variety of factors contributes to peritoneal inflammation and bacterial growth in ascitic fluid. A key predisposing factor may be the intestinal bacterial overgrowth found in people with cirrhosis, mainly attributed to delayed intestinal transit time. Intestinal bacterial overgrowth, along with impaired phagocytic function, low serum and ascites complement levels, and decreased activity of the reticuloendothelial system, contributes to an increased number of microorganisms and decreased capacity to clear them from the bloodstream, resulting in their migration into and eventual proliferation within ascites fluid.

Interestingly, adults with spontaneous bacterial peritonitis typically have ascites, but most children with spontaneous bacterial peritonitis do not have ascites. The reason for and mechanism behind this is the source of ongoing investigation.

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Etiology

Traditionally, three fourths of spontaneous bacterial peritonitis infections have been caused by aerobic gram-negative organisms (50% of these being Escherichia coli). The remainder has been due to aerobic gram-positive organisms (19% streptococcal species). E coli is displayed in the image below.

Gram-negative Escherichia coli.

However, some data suggest that the percentage of gram-positive infections may be increasing.
[2, 3] One study cites a 34.2% incidence of streptococci, ranking in second position after Enterobacteriaceae.
[3] Viridans group streptococci (VBS) accounted for 73.8% of these streptococcal isolates.

Anaerobic organisms are rare because of the high oxygen tension of ascitic fluid.

A single organism is noted in 92% of cases, and 8% of cases are polymicrobial.

Risk factors

Patients with cirrhosis who are in a decompensated state are at the highest risk of developing spontaneous bacterial peritonitis.
[4] Bacterial translocation (viable microorganism passage from the intestinal lumen to mesenteric lymph nodes) is a key factor in the development of spontaneous bacterial peritonitis.
[5] Low complement levels are associated with the development of spontaneous bacterial peritonitis. Patients at greatest risk for spontaneous bacterial peritonitis have decreased hepatic synthetic function with associated low total protein level or prolonged prothrombin time (PT).

Patients with low protein levels in ascitic fluid (< 1 g/dL) have a 10-fold higher risk of developing spontaneous bacterial peritonitis than those with a protein level greater than 1 g/dL.

A 2014 prospective study by Terg et al
[6] demonstrated that proton pump inhibitor therapy (specifically evaluated at admission) was not associated with a higher risk of spontaneous bacterial peritonitis. This finding was contrary to findings by previously published studies (2012 review by Siple et al
[7] and a 2013 study by Deshpande et al
[8] , which had reported several case studies and cohorts of patients with cirrhosis and chronic liver disease who were on proton pump inhibitors (PPIs) for a prolonged duration who were at significantly increased risk for the development of spontaneous bacterial peritonitis. .

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Epidemiology

In patients with ascites, the frequency may be as high as 18%. This number has grown from 8% over the past 2 decades, most likely secondary to an increased awareness of spontaneous bacterial peritonitis and a lowered threshold to perform diagnostic paracentesis.

No race predilection is known for spontaneous bacterial peritonitis. In patients with ascites, both sexes are affected equally.

Although the etiology and incidence of hepatic failure differ between children and adults, in those individuals with ascites, the incidence of spontaneous bacterial peritonitis is roughly equal. Two peak ages for spontaneous bacterial peritonitis are characteristic in children: the first in the neonatal period and the second at age 5 years.

According to a 2015 study by Ge and Runyon, when the initial infection was spontaneous bacterial peritonitis, subsequent infections were more likely to be caused by drug-resistant organisms. The risk of subsequent infections was increased in older patients and in patients taking proton-pump-inhibitors (PPIs) or spontaneous bacterial peritonitis prophylaxis (ie, selective intestinal decontamination).
[9]

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Prognosis

The mortality rate in patients with spontaneous bacterial peritonitis ranges from 40-70% in adult patients with cirrhosis. Rates are lower in children with nephrosis. Patients with concurrent renal insufficiency have been shown to be at a higher risk of mortality from spontaneous bacterial peritonitis than those without concurrent renal insufficiency. Mortality from spontaneous bacterial peritonitis may be decreasing among all subgroups of patients because of advances in its diagnosis and treatment. In addition, nonselective beta-blockers increase the risk for hepatorenal syndrome and death in patients with cirrhosis and spontaneous bacterial peritonitis.
[10]

Growing evidence supports early diagnostic paracentesis (defined as occurring within the first 11 hours of presentation). This, combined with early antibiotic treatment, leads to decreased ICU and hospital length of stay, in-hospital mortality, and 3-month mortality.
[11, 12]